Not a doctor either but just wanted to say that weaning yourself off can do more harm than good...I tried it after being PVC free for three years on 25mg Atenolol and having a problem ever since.
Just one person's opinion but if you find something that works...DON"T change it!!!!!
PS. I realise this question was directed to the doctor but just thought I'd give my 2 cents since it's on this board.
Sorry, Just to correct my second paragraph, it should read:
This in the literature too. People with slow rate dependent PVCs (MORE PVCs at night) had an increase on beta blockers, people with high rate dependent PVCs (FEWER PVCS at night) had a decrease.
My cardiologist told me that some people have heart rate dependent PVCs and these can definitely be made worse by beta blockers, which lower the heart rate. It does seem to make sense.
This in the literature too. People with slow rate dependent PVCs (fewer PVCs at night) had an increase on beta blockers, people with high rate dependent PVCs (more PVCS at night) had a decrease.
This study was conducted at the Institute of Cardiology, University of Bari. Published in European Heart journal.
I haven't seen the whole paper though so I can't say whether their statistical analysis was up to scratch. They may not done have done enough holters to determine the normal degree of variation and therefore whether their findings are statistically significant.
It has been reported that the frequency of premature ventricular contractions in some patients tend to decrease during the hours of sleep when modifications in autonomic tone and bradycardia occur. The aim of this study was to evaluate whether the phenomenon of sleep suppression may be a sensitive and specific parameter for predicting the antiarrhythmic effect of beta-blockers on premature ventricular contractions. The presence of sleep suppression was evaluated in 45 patients (mean age 50 +/- 17 years) with frequent premature ventricular contractions at two baseline Holter recordings. Sleep suppression was defined as > 50% reduction in the number of nighttime as opposed to day-time premature ventricular contractions. Three groups of patients were identified: those with sleep suppression at both Holter recordings (group 1); those with sleep suppression at only one Holter recording (group 2); and those without sleep suppression at either Holter recording (group 3). A third Holter was performed 5 days after nadolol administration. In group 1, nadolol led to a mean reduction in the number of premature ventricular contractions of 90% (> 70% in 21/23 patients). In group 2, the mean reduction was 76% (> 70% in three out of six patients). In group 3, there was a mean increase in the number of premature ventricular contractions of 33%. The positive predictive accuracy of sleep suppression in relation to the antiarrhythmic efficacy of nadolol is very high (88%) when sleep suppression is present during two baseline Holter recordings. Sleep suppression is a sensitive parameter for identifying the premature ventricular contractions likely to benefit from beta-blocker administration.